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Gene Review

VV  -  varicose veins

Homo sapiens

 
 
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Disease relevance of VV

 

Psychiatry related information on VV

 

High impact information on VV

 

Chemical compound and disease context of VV

 

Biological context of VV

  • The combined phenotype of having VV and H did not show any evidence of linkage or association [20].
  • Linkage to the FOXC2 region of chromosome 16 for varicose veins in otherwise healthy, unselected sibling pairs [20].
  • Interestingly, re-phosphorylation of SR-VV proteins only partially restored the splicing enhancer or splicing repressor phenotype to the SR proteins [21].
  • By infecting nonpermissive cells with this library and screening for VV gene expression and replication, we isolated a virus containing a 2.8-kb HCMV fragment that rescues replication of VVdeltaE3L [22].
  • Individuals with the VV homozygous mutant genotype thus had the highest plasma levels of homocysteine [15].
 

Anatomical context of VV

  • BACKGROUND: The addition of long saphenous vein (LSV) stripping to sapheno-femoral junction (SFJ) disconnection and multiple stab avulsions (MSAs) in the course of varicose vein (VV) surgery is associated with a significant reduction in recurrence, and a significant improvement in quality of life [23].
  • VV were defined as dilated, tortuous and elongated veins of the lower extremities and were classified into four types [4].
  • The prevalence of VV was significantly higher among patients with CAE (40%) compared to 200 aged-matched patients with coronary artery disease but without CAE (17%) and to 201 randomly selected subjects from the general population (23%) [24].
  • Clinical observations suggest that varicose veins (VV) are less frequent in patients undergoing infrainguinal bypass surgery for femoral artery occlusive disease [25].
  • Piles are caused by varicose veins in the anal canal [26].
 

Associations of VV with chemical compounds

 

Physical interactions of VV

  • CONCLUSION: the reduced endothelin-1 binding and endothelin-B receptor density may be partially responsible for the reduced vasocontractility in varicose veins [32].
  • We conclude that the cellular hypertrophy of the SMC and the microherniations could be the basis for disruption of the elastin fibers connected to the SMC in varicose veins [33].
 

Regulatory relationships of VV

 

Other interactions of VV

  • RESULTS: Levels of tPA were significantly higher at the groin (11 +/- 2) than the ankle (5 +/- 1) in the VV (p < 0.005), and this trend was also seen in the NV (groin 10 +/- 2 and ankle 7 +/- 3) [27].
  • Levels of uPA were significantly higher in the groin VV (14 +/- 4.3) than in NV (3.0 +/- 0.8, p < 0.05) [27].
  • CONCLUSION: A significant increase in the collagen content and a significant reduction in the elastin content of VV were demonstrated [39].
  • Increased TIMP/MMP ratio in varicose veins: a possible explanation for extracellular matrix accumulation [40].
  • Characterization of endothelin receptors in human varicose veins [41].
 

Analytical, diagnostic and therapeutic context of VV

  • We hypothesised that this gene might be implicated in the development of VV in the normal population, therefore, after performing a classical twin study, we tested for linkage and association in white women [20].
  • It has been suggested that concomitant ligation of the vertical vein (VV) is not necessary in the repair of total anomalous pulmonary venous connection [42].
  • Most surgeons (n = 168, 77.1%) reserved sclerotherapy for residual VV postoperatively [43].
  • HRT users were significantly thinner (27% with body mass index (BMI = (kg/height (m2)) > or = 27 vs. 41%, p = 0.04) and less likely to have a history of DVT (12 vs. 33%, p = 0.02) and varicose veins (VV) (52 vs. 69%, p = 0.04) than non-users [44].
  • OBJECTIVES: The purpose of this study was to examine the differentiation of gene expression in the wall of VV using complementary deoxyribonucleic acid (cDNA) microarrays [45].

References

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  15. Genetic polymorphism of 5,10-methylenetetrahydrofolate increases risk of myocardial infarction and is correlated to elevated levels of homocysteine in the Japanese general population. Nakai, K., Fusazaki, T., Suzuki, T., Ohsawa, M., Ogiu, N., Kamata, J., Kawazoe, K., Nakai, K., Itoh, C., Yanagisawa, M., Ishida, T., Hiramori, K. Coron. Artery Dis. (2000) [Pubmed]
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  21. Functional inactivation of the SR family of splicing factors during a vaccinia virus infection. Huang, T.S., Nilsson, C.E., Punga, T., Akusjarvi, G. EMBO Rep. (2002) [Pubmed]
  22. Evasion of cellular antiviral responses by human cytomegalovirus TRS1 and IRS1. Child, S.J., Hakki, M., De Niro, K.L., Geballe, A.P. J. Virol. (2004) [Pubmed]
  23. The effect of long saphenous vein stripping on deep venous reflux. MacKenzie, R.K., Allan, P.L., Ruckley, C.V., Bradbury, A.W. European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery. (2004) [Pubmed]
  24. Varicose veins are common in patients with coronary artery ectasia. Just a coincidence or a systemic deficit of the vascular wall? Androulakis, A.E., Katsaros, A.A., Kartalis, A.N., Stougiannos, P.N., Andrikopoulos, G.K., Triantafyllidi, E.I., Pantazis, A.A., Stefanadis, C.I., Kallikazaros, I.E. European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery. (2004) [Pubmed]
  25. Are varicose veins a marker for susceptibility to coronary heart disease in men? Results from the Normative Aging Study. Scott, T.E., Mendez, M.V., LaMorte, W.W., Cupples, L.A., Vokonas, P.S., Garcia, R.I., Menzoian, J.O. Annals of vascular surgery. (2004) [Pubmed]
  26. Piles are caused by varicose veins in the anal canal. Watts, G.T. Lancet (1986) [Pubmed]
  27. Plasminogen activator levels are influenced by location and varicosity in greater saphenous vein. Shireman, P.K., McCarthy, W.J., Pearce, W.H., Shively, V.P., Cipollone, M., Kwaan, H.C., Yao, J.S. J. Vasc. Surg. (1996) [Pubmed]
  28. Prevalence of varicose veins in an Italian elderly population. Canonico, S., Gallo, C., Paolisso, G., Pacifico, F., Signoriello, G., Sciaudone, G., Ferrara, N., Piegari, V., Varricchio, M., Rengo, F. Angiology. (1998) [Pubmed]
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  30. Primary defect in alpha-adrenergic responsiveness in patients with varicose veins. Blöchl-Daum, B., Schuller-Petrovic, S., Wolzt, M., Korn, A., Böhler, K., Eichler, H.G. Clin. Pharmacol. Ther. (1991) [Pubmed]
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  32. Endothelin receptors in the aetiology and pathophysiology of varicose veins. Agu, O., Hamilton, G., Baker, D.M., Dashwood, M.R. European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery. (2002) [Pubmed]
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  40. Increased TIMP/MMP ratio in varicose veins: a possible explanation for extracellular matrix accumulation. Badier-Commander, C., Verbeuren, T., Lebard, C., Michel, J.B., Jacob, M.P. J. Pathol. (2000) [Pubmed]
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  43. A survey of current attitudes of British and Irish vascular surgeons to venous sclerotherapy. Galland, R.B., Magee, T.R., Lewis, M.H. European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery. (1998) [Pubmed]
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  45. Gene expression profiles in varicose veins using complementary DNA microarray. Lee, S., Lee, W., Choe, Y., Kim, D., Na, G., Im, S., Kim, J., Kim, M., Kim, J., Cho, J. Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]. (2005) [Pubmed]
 
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